Objective In order to provide the basis for establishment of food allergy models , we compared the differences of sensitivity and alterations of intestinal flora of food allergy models in two strains of mice .Methods Forty 4-5-week old female BALB/c and Kunmimg mice were divided into control group ( n=10) and food allergy goup ( n=30), respectively.Ovalbumin (OVA) was injected to the mice to establish food allergy models .Serum OVA-specific IgE of the mice was assayed by ELISA .The jejunum tissue was examined by pathology with HE staining .The changes of fecal flora were detected by denaturing gradient gel electrophoresis (DGGE).Results (1)Among the sensitized 60 mice, OVA-sIgE levels were significantly increased in 27/30 BALB/c mice and 21/30 KM mice compared with those of control groups(P<0.001).Moreover, there were more evident inflammatory cell infiltration , epithelial cell shedding and cytolysis in the jejunal villi of BALB/c mice than those of KM mice.(2) After food allergy modeling, there were significant changes of intestinal flora in the BALB/c mice (P<0.001), while only significant change of evenness was found in the KM mice (P<0.05).(3)There were changes of abundance , Shannon index and evenness of intestinal flora in the model groups of BALB/c and KM mice.Conclusions BALB/c mice are more sensitive to OVA allergy than KM mice .The composition of intestinal flora is different among different strains of mice .The changes of intestinal flora after OVA challenge in BALB /c mice are more obvious than those in KM mice .

Radiotherapy can cause functional and morphological changes in the brain tissues of patients with primary or metastatic malignant brain tumors, leading to radiation-induced brain injury. However, the pathogenesis of radiation-induced brain injury has not yet been unanimously determined, and its research advances and treatment protocols are yet to be elucidated and improved. In this study, we explore the pathogenesis of radiation-induced brain injury from the perspective of vascular injury, inflammatory reactions, neuronal dysfunction, glial cell injury, and gut microbiota and reviewed the advances in research on its treatment and prevention. The purpose is to provide a reference and theoretical basis for the research and clinical diagnosis and treatment of radiation-induced brain injury.

The oral microbiota is associated with oral diseases and digestive systemic diseases. Nevertheless, the causal relationship between them has not been completely elucidated, and colonisation of the gut by oral bacteria is not clear due to the limitations of existing research models. The aim of this study was to develop a human oral microbiota-associated (HOMA) mouse model and to investigate the ecological invasion into the gut. By transplanting human saliva into germ-free (GF) mice, a HOMA mouse model was first constructed. 16S rRNA gene sequencing was used to reveal the biogeography of oral bacteria along the cephalocaudal axis of the digestive tract. In the HOMA mice, 84.78% of the detected genus-level taxa were specific to the donor. Principal component analysis (PCA) revealed that the donor oral microbiota clustered with those of the HOMA mice and were distinct from those of specific pathogen-free (SPF) mice. In HOMA mice, OTU counts decreased from the stomach and small intestine to the distal gut. The distal gut was dominated by Streptococcus, Veillonella, Haemophilus, Fusobacterium, Trichococcus and Actinomyces. HOMA mice and human microbiota-associated (HMA) mice along with the GF mice were then cohoused. Microbial communities of cohoused mice clustered together and were significantly separated from those of HOMA mice and HMA mice. The Source Tracker analysis and network analysis revealed more significant ecological invasion from oral bacteria in the small intestines, compared to the distal gut, of cohoused mice. In conclusion, a HOMA mouse model was successfully established. By overcoming the physical and microbial barrier, oral bacteria colonised the gut and profiled the gut microbiota, especially in the small intestine.
Animals ; Bacteria ; Gastrointestinal Microbiome ; Germ-Free Life ; Humans ; Mice ; Microbiota ; RNA, Ribosomal, 16S